Topic
Iodine
About: Iodine is a research topic. Over the lifetime, 8936 publications have been published within this topic receiving 139981 citations. The topic is also known as: I & element 53.
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TL;DR: Administration of iodine during the first 10 weeks of life increased the incidence of the disease, as determined by histology and the measurement of autoantibodies to triiodothyronine, thyroxine, and thyroglobulin.
Abstract: Clinical studies have suggested that excess dietary iodine promotes autoimmune thyroiditis; however, the lack of a suitable animal model has hampered investigation of the phenomenon. In this study, different amounts of potassium iodide were added to the diets of chicken strains known to be genetically susceptible to autoimmune thyroiditis. Administration of iodine during the first 10 weeks of life increased the incidence of the disease, as determined by histology and the measurement of autoantibodies to triiodothyronine, thyroxine, and thyroglobulin. Further support for the relation between iodine and autoimmune thyroiditis was provided by an experiment in which iodine-deficient regimens decreased the incidence of thyroid autoantibodies in a highly susceptible strain. These results suggest that excessive consumption of iodine in the United States may be responsible for the increased incidence of autoimmune thyroiditis.
174 citations
TL;DR: In this paper, it was shown that methyl iodide is a major contributor to the flux of iodine from the ocean to the atmosphere, but its sources in the ocean are largely unknown, except for production by certain species of coastal macrophytic algae.
Abstract: It is generally accepted that methyl iodide is a major contributor to the flux of iodine from the ocean to the atmosphere, but its sources in the ocean are largely unknown, an exception being production by certain species of coastal macrophytic algae. Preliminary results reported here indicate production of methyl iodide in filtered seawater that has been irradiated with either sunlight or an artificial light source having a spectral output closely approximating to sunlight at sea level. The production was enhanced when the water samples were deoxygenated and by the addition of iodide to this water. The results appear to be consistent with a mechanism involving reaction between photochemically produced methyl radicals and iodine atoms. It is estimated that the process is capable of making a significant contribution to global iodine fluxes.
173 citations
172 citations
TL;DR: In this paper, it was shown that thiols were effectively oxidized into disulfides by reacting with hydrogen peroxide in the presence of a catalytic amount of iodide ion or iodine.
Abstract: Thiols were effectively oxidized into disulfides by reacting with hydrogen peroxide in the presence of a catalytic amount of iodide ion or iodine.
171 citations
TL;DR: Thyroid hormone formation requires the coincident presence of peroxidase, H2O2, iodide, and acceptor protein at one anatomic locus in the cell, and clinical problems involving defective per oxidase function are among the most frequent hereditary defects of thyroid hormone formation.
Abstract: Thyroid hormone formation requires the coincident presence of peroxidase, H2O2, iodide, and acceptor protein at one anatomic locus in the cell. The peroxidase enzyme appears to be a protoporphyrin IX containing heme protein, with binding sites for both iodide and tyrosine. It is probable that both iodide and tyrosine are oxidized to free radical forms which unite to form iodotyrosine. The peroxidase is also involved through an uncertain mechanism in iodotyrosine coupling and probably in oxidation of sulfhydryl bonds in thyroglobulin. H2O2 may be supplied by microsomal NADPH-cytochrome c reductase or NADH-cytochrome b5 reductase. Other possible intracellular H2O2 generating systems include monoamine oxidase and xanthine oxidase. The usual acceptor for iodide is thyroglobulin, which is currently believed to be iodinated within apical secretory vesicles at the cell border just prior to liberation into the colloid, or possibly after liberation into the colloid. Other soluble and insoluble proteins are also iodinated within the gland. The peroxidase is present in numerous cellular structures, but iodination activity occurs primarily, if not only, at the apical cell border. The controls of iodination are imperfectly known. Thyrotrophin modulation of iodide uptake, H2O2 generation, thyroglobulin synthesis, and peroxidase enzyme level obviously are the main regulations. Many of these actions are thought to involve mediation of adenyl cyclase and subsequent activation of intracellular phosphokinases. Antithyroid drugs of the thiocarbamide group are competitive inhibitors of iodination under some circumstances, but if much iodide is present, they react with the oxidized iodine intermediate and are irreversibly inactivated themselves. Clinical problems involving defective peroxidase function are among the most frequent hereditary defects of thyroid hormone formation. Recognized abnormalities include deficient peroxidase, abnormality in binding of the peroxidase apoprotein to its prosthetic group, and other less well-identified abnormalities in peroxidase structure and function. Peroxidase is typically elevated in thyroid tissue from patients with hyperthyroidism, sometimes deficient in cold thyroid nodules, and frequently diminished in tissue from patients with Hashimoto's thyroiditis.
170 citations